First I have to apologize for my back lag of answering emails and forum posts. I am still trying to catch up after being 3 days out of order due to a hip operation and I slowly try to catch up on patients, emails and on here. So here not as an excuse but as a " time saver". I got over the last 3 - 4 weeks an incredible number of very nice and positive e mails. Readers out there seem to start to get some fun on what we do here and in many cases start to actually think in a great way to enhance what we do and like to try to get over as a message. So to summarize a big group of mails : MOXY seems to have an incredible potential ( My add on NIRS ) . Problem with the forum. YOU ( Which is me ) run often away with far to much into detailed discussion and answers with some regular readers, who are now as well far ahead of the majority of new readers and as such the new comber looses connection and opportunities to come back with very basic questions on MOXY My simple answer to this is: You are all absolutely right. I am always getting back into the same stupid habit to try to show all and more what is possible and often than talk in " our " language and therefor loose many great opportunities to invite more people in our small world of practical application and physiological thinking.

Okay give me another chance and than many more as I am sure I will get lost again. So please simply insist and come back and bug me.

I like to use a Case study here :Target readers: Newcomers, personal coaches . PE teachers, Fitness center owners. Small interest groups in any endurance sport. Sport stores and more.Goal: Show a very basic nearly " classical " use of MOXY. Many of the above group have all one question and problem in common: How can I use physiological testing ideas for my group or myself. a) Invasive blood testing like lactate has some legal problems and some fear for many people of contamination, as well as there are more and more readers questioning the benefit of lactate testing in a group setting or even as a field test methodb) VO2 testing is interesting, somewhat lab specific and you often can do one by one only. Still some possible contamination problem with masks and all the limitation we often discussed. Main problem for sure is the price. A decent good VO2 equipment is somewhere between 6'000 $ and up. And it can only be used for the testing . So the majority off mails clearly indicate, that MOXY is now a very affordable equipment of the above groups and many even ask , whether it would make sense to have 4 or more units. H ahaa I am biased. So my best answer is here. Start with one learn to see what you will do with it and than you still have 5'000 $ left for what ever you like to add later.

Basic case we look at:It is a simple step test done outdoors in running with a GPS guided speed control. There is many other I options if you do not have a GPS for speed control we can discuss later.Test is 5 min step test . Start speed 3 mph . Speed increase very 5 min 1 mph till subjective feeling that is it. The run was done on a relative flat road around the neighbor hood. As usual I get many data's and the only part I use is to not read any comment and just take the MOXY csv file to look at this first. If we have HR with it great or speed great. But I like to concentrate just on what we get out of MOXY.

So let's start with the SmO2 information. SmO2 is given in % as an absolute number. It is the % of Hb ( Mb ) loaded with oxygen.Simple example. 100 Hb pieces. and 65 of this Hb ( Mb ) are loaded with O2 so O2Hb ( loaded hemoglobin or oxyhemoglobin are loaded and 35 HHb deoxyhemoglobin are not loaded and SmO2 is 65 %. In MOXY " language" red is used for O2Hb, blue is used for HHb, green is used for SmO2. Now O2Hb plus HHb will give you 100 and it is the tHb ( total hemoglobin ) We use a brown color for tHb. Basic interpretationSmO2: An increase in SmO2 indicates that we deliver more O2 to the test area than we for the current intensity actually would need .a flat SmO2 trace indicates, that for the current situation we have in the test area a balanced situation, where the amount of O2 delivered equals the amount of utilized Oxygen.a dropping SmO2 trace indicates that at that current situation in the test area the oxygen used is higher than the amount who can be or is delivered. In other words we have in this case a " time " situation on how long we can afford to use more than we can deliver.? Okay your turn. Let's make an interpretation based on the above.You explain. every grid line ( 300 is 300 seconds so approximately 5 min change off speed . first 0 - 300 is 3 mph and than every time 1 mph faster. So how many complete steps did he do ? Some interesting points. VL and D ( delta ) have a relative similar trend at least the first 2 steps. The gastrocnemius ( calf ) seem to have a mind on its own. Now in running the running speed can have an incredible influence on the calf activity as in a very slow speed and here it is 3 mph you run very different , than when you run 5 or 6 mph. Actually really can we " run" 3 mph " well for sure but interesting enough that would be for most of us fore foot running even if we are heel striker as it is so slow that you have some major problem to run over your heel if you are a heel striker.Now IF this would be the case here we would have a very rapid drop in SmO2 on the calf but we do not have that really . We see that drop by step 3. So the question comes up , whether in this case step one and 2 because of the slow pave where actually done in walking so very little calf activity as we are clear heel striker. ?Than by step three clear drop so possible as well from the speed slow jogging and we have a confirmation form the vastus lateralis as he has to work harder now when we jog than walk. Now go from calf to VL to D and try where you would be able to see some relative clear reactions inSmO2 trend. One more interesting point is the step 4 , where at least the D suggests , that there was a moment of a higher speed followed by a possible correction of speed .? If we have speed feedback or even HR we would have the answer. So below I show you some suggestion of " zoning" 1. VL SmO2 trendSeems to be relative straight forward. We always could discuss HII ( High intensity ) I chose HII as he was not able to finish the 5 min as it looks

Now same idea for calf.Some what not happy. Now this is very subjective, but after all this years of using NIRS I never be happy with the calf muscle feedback . Sometimes it seem to work nicely but in many cases the trend is not optimal like in this case. There are many reason for this , so I do not use MOXY on the calf. The only possible reason why people like it is , that it is relative easy for placement. If people have tights on you can simply push the lower part up which is for many people more comfortable than pushing your pants down ( Smile ) most likely it is easier to run with the pants up than with the pants down. If you do not believe that try it out ( But sent us the video )

So we look at the third MOXY placed on the front delta portion. So this muscle is actually involved in running, but much less important so least involved muscle.

Nearly the nicest trend. Step 4 the questionable drop and recovery and steep 5 a small similar situation as well. I added with some rough look at the HR the potential HR " zoning " to it.

Now that is it Your basic ' Individual ZONING idea based on SmO2 trend and than using HR or speed ( performance to guide the workouts. In most cases we may use the familiar HR as HR monitors are all over in any fitness person. Nothing is calculated nothing is % it is all feedback from your body. Optimal < Using HR and MOXY and you can daily have your planned optimal zone based on live feedback from HR and SmO2 and sometimes respiratory frequency. That is it. I will add a next thread for the advanced use of this case study and than perhaps a third for the Pro user.

Advanced use:In the advanced use idea we integrate tHb to it. tHb as an indication in many cases on the blood flow in the tested area. Here the overall view

tHb can be influenced by different physiological reactions.To make it again simple. A decrease in tHb could be named vasoconstriction or reduction in blood flow. Vasoconstriction can have in simple terms 2 reasons. 1. Mechanical reason . like muscle contraction so we compress the blood vessels and we reduce blood flow so tHb drops ( similar like when we inflate a BP cuff.. So we have first a reduce v blood flow so tHb drops. If we keep pumping up we half suddenly a pressure , which stops outflow venous occlusion or at least reduces outflow, so despite a initial compression we now may see an increase in tHb as blood still moves in but less or nothing moves out.. If we let go the cuff or muscle compression than we see a drop as we have now first a pooling outflow before we are back to " normal " flow. If we even increase more we may reach an in and anyway outflow pressure and now tHb is flat. ( so it looks like normal but when we let go we see first a drop as again an outflow ( some exceptions ).There is one more easy way to see, whether it is a complete occlusion or free flow. Look and think what you may expect SmO2 would do under complete occlusion versus free flow.Now lets go again from muscle to muscle and you make the interpretation.

Vastus lateralis. Now I added SmO2 to it so it is easier to make some conclusions.

Nice isn't it and that's' all out of the small unit. Tell yourself honest. What can you read even remote close to what we see here form a VO2 max test or a Maximal HR test or even worse a formula of age related to potential Max HR ?? Now next is calf muscle

And last the delta information

Now you can see in the delta that there was a clear change in speed in step 4

Now I like to finish the advanced section with the explanation , why in many cases a simple mount of the moxy on the arm is the fastest best way to do. Push the sleeve up and mount it there. I have for myself a shirt with a build in section so I can simply push the shirt in. No PR for the shirt company here. Smile . For cyclists you simply build it into the cycling shorts

Here the explanation why it works.We had it many times and we backed it up with some great studies form different section of medicine.

So much for the advanced readers. Now lets see in the next thread whether we can challenge the pros in our reader group.

Pro interpretation Bad wording our Pro's do not need an interpretation, they simply need some additional pictures to the once we had before. Okay here we go. I would argue , that this person has a good delivery system and has a limitation in vascularisation, and as such mitochondria density. Now remember. we normally use a 5/1/5 and in that idea the one minute rest to try to find the limiter and compensator as it repeats it every 4 5 min. What repeat's its elf. The nice situation, where we suddenly completely stop[ O2 demand form working muscles but we keep up for a certain lag time the delivery for this O2 demand. Than we start suddenly and now we have a huge demand but not anymore a great delivery which again has a lag time befog it picks up. Now in a 5 min step test we have both situations once ??Now look at advanced pictures and use SmO2 tHb from VL or even from calf muscle. Than we can add more and here is a biased feedback form all there muscles . You make the interpretation.

VL biased

Calf biased

Delta biased

Biased means here. That we look O2Hb and HHb trend as it develops over the test by assuming that both are equal at thee start so 0. This show s us nicely whether and what happens during the test on relative change in O2 in each step.

Now you add HR and performance and in many cases easy RF to it and you have a physiological test with a physiological feedback clearly into much more depth than anything we use or used in the past for a fraction of equipment easy to use for any body and anywhere and in any sport.

Thank you from all the "beginners" out there. I have some questions regarding the analysis. I'll start with the first graph and then move on.

So the SmO2 graphs and zoning for each of the muscles. I understand how the basic zonings are figured out based on basic trends...rising SmO2-ARI, stable SmO2-STEI, dropping SmO2-FEI and then the HII maybe a tough one on this...

Now for vascularization development, I read on the forum or in the pdf's that training at the highest point of SmO2 would be valuable...why not at the highest intensity of the STEI zone?...is it the high O2 content within the muscle that triggers the stimulus for capillarization...then how about mitochondrial density?...why not the highest intensity of STEI zone therefore putting a stress on enzymatic activity, mitochondrial activity?

Now the dropping FEI zone would indicate an increased demand for O2 but decrease in ability to supply it (via cardiac or respiratory or maybe the delivery men?)...however can this dropping Sm02 be a result of poor capillarization?mitochondrial density?...how can we tell the difference between the supplying part being a limiter vs. the using parts (enzymatic or mito)

Okay, maybe too many questions for the beginner part...one more thought:

the speed check in step four...my interpretation based on looking at the tHb would be that the subject started the step too fast, hence the drop in tHb in the deltoid (blood moved away from least involved muscle) and then once the speed was correct it went back up...

In a little bit I'll come back with questions regarding the "advanced" interpretations...tHb stuff and occlusions...

Thanks Dan , Here a try to give some feedback and some even may be actual answers . Sorry but I write a lot ans sometimes it may be smart sometimes more confusing. so here your question where I need some help:

I read on the forum or in the pdf's that training at the highest point of SmO2 would be valuable

I am nor sure but I can't remember nor would I have the courage top give an answer on how coaches out there with much more experience suppose to train vascularisation and mitochondria density. This is up to the coaches to do that. We simply supply a tool so coaches can see what is limiter and what is compensator. In the past they did not had this now they know after a test what has to be improved and now they can create a training plan based on this directions and goals rather than on % of something.. But again can you show me what the heck I may have written in a pdf or on the forum. on how to stimulate mitochondria density and capillarisation.

2. Now the dropping FEI zone would indicate an increased demand for O2 but decrease in ability to supply it (via cardiac or respiratory or maybe the delivery men?)...

I am not sure whether we can do this that simple and that is the risk when going too basic. So here my take. A dropping SmO2 .where we use to make the ideas, that this is in FEI, can have different reasons.a) Same O2 demand but less supply than before so SmO2 drops.. Could be seen in tHb reaction. So same CO perhaps even same HR and Same SV but more muscle compression. Or Same CO but lower SV and higher HR and more muscle compression and many more options.

b) Higher O2 demand and higher O2 delivery, but the demand is higher than the even increased delivery can handle so SmO2 is dropping as well as well.

c) your suggestion as a decrease in delivery and an increase in demand so SmO2 drops.

d) same delivery but higher demand so SmO2 drops.

This options will help you do get more feedback on limiter and compensator. So that would lead to some thoughts on your last part

however can this dropping Sm02 be a result of poor capillarization?mitochondrial density.

poor capillarisation could be a part of poor delivery ability or as capillarisation is a part of the delivery system . SmO2 is a part of the energy delivery idea so O2 % of the tHb.. Whether we have a great loaded Hb depends mainly on the exchange area in the lungs to the blood. Once it is in the blood it will be somehow delivered. . If we have a great CO and a good respiration ( CO2 balanced than we have a good loaded blood SpO2. Now the delivery is no dependent on the blood vessels and as such on the ability to utilize it in the mitochondria..So a poor capillarisation and a low mitochondria density would not change the amount of O2 I have loaded , in fact it may be that I have a great CO and optimal loading, and I load so much , that I not or barely will see a dent in the utilization if there is a poor mitochondria density.. That is the reason why we have in many cases a very interesting situation. A top endurance athlete and I work for the moment with a 100 - 150 mile runner, barely shows a drop in SmO2 and he can go long and long relative fast long meaning over 10 plus hours and fast meaning 5 min / km and faster for that duration. His deliver when we test him is incredible and his ability to move on FFA and using O2 as well but he is in complete balance after " warm up where he is " fully moving O2 and his is balanced in his race speed. Interestingly enough barely can handle changes in speed otherwise , he runs into trouble.

On the other side we have very healthy but very untrained people. Their delivery system is not great but healthy an good enough to delver far more than they can utilize or turn around. So same picture as we see an increase in SmO2 an than minimal sometimes no drop in SmO2 even in an all out intensity.

Like poor CO is a part of poor or lets put it more positive not optimal delivery. Sop the question is, whether when I have a low mitochondria density , whether SmO2 drops really as I simply turn around what i get delivered. As O2 only can drop or possibly only can drop if it is used it seems to me it depends on mitochondria activity and as well density.. So low density no drop of O2 as it is not utilized. Hmm does that makes sense..The other interesting part is as well that mitochondria density is directly connected with capillarisation. The ability to use O2 can be dependent on the mitochondrial activity. So to create in simple terms more mitochondria I have to develop first more blood vessels.

But I can improve mitochondrial utilization without more mitochondria and than I can turn more energy , around as well.

That is the every 15 years new discussion between HIT and LSD. A very high intensity training and much research shows that over 6 - 8 weeks is more successful in using O2 than a LSD for 6 - 8 weeks.

So the conclusion we than learn is HIT is better than LSD and it is used as a great fitness PR for centers. Go short and hard an you will have the same end result as when you go long or slow actually even better as you do not " waste " time. Than EPOC moves in it an you have a very Gospel like group of people running for that.

LSD over 6 - 8 weeks shows limited changes as it is an intensity, where a lot of structural changes take place like for example vascularisation or numbers of mitochondria.. There are ample of research done showing this BUT you have to look at studies over 3 -5 and more years. If you go all out HIT and this is the only traininig your do you see great and fast improvement for 6 - 8 Weeks. Do the same for 16 - 18 weeks and than for 3 - 4 years and compared with the once who do a lot of LSD ( and see, how they stake up now.

Problme : I can not find , so please help. A HIT research. where they did the HIT over a 3 -4 years duration and than compared with the LSD idea. On the other side we have even longer studies on LSD from cross counrty skiing and rowing, where in this sports 80 +0- % of the time invested is done in a LSD or they use lactate as a no show for their LSD as it is still produced but it is turned around and does not show up in the finger or ear. If and just IF we can do a 20 min HIT and than go and win a 50 km cross country skii or a Tour de france, may allow to ask the question, why all this pros train so much and so long and so slow. Will try to fond ome stduie s who show tweh ratio of LSD to HIT in endurance sport.

This discussion may answer Dan's first question on STEI and intensity versus high SmO2. What is your goal : Functional versus structural ? Here a little bit more to start.

Structural and functional adaptations of the cardiovascular system by training.

Muscular training induces structural and functional adaptations within the cardiovascular system which vary according to type, intensity and duration of muscular exertion. Dynamic muscular training for more than 5 h a week involving more than 1/6th of the skeletal muscle mass causes an increase in parasympathetic tone and an eccentric myocardial hypertrophy. The dimensions of all cardiac chambers enlarge up to 20% and the cardiac muscle mass may increase by 70%-80%. Static muscular training does not induce any change in the parasympathetic heart regulation, nor does it lead to any disproportional increase in cardiac muscle mass relative to skeletal muscle mass. However, a tendency towards a concentric myocardial hypertrophy can be observed. The effects of regular muscular training on the arteries are the subject of current scientific investigation. To explain the acute and chronic adaptations of the arterial vasculature to exercise, a "shear stress" hypothesis has been proposed. During dynamic muscular exercise the regional arterial blood flow is enhanced. This leads to an acute increase in intraluminal shear forces, which stimulates the vascular endothelium with a reactive flow-dependent regional vasodilation mediated by endothelial-derived relaxing factors (EDRF, EDNO). Chronic enhancement of shear forces induces endothelial cell-mediated alterations in gene expression (endothelin, growth factors, regulators of fibrinolysis) and chronic structural adaptations of the vascular wall (cytoskeletal redistribution, cell shape change). Recent duplex sonographic studies in humans have revealed a significant lumen increase of muscular type arteries induced by dynamic, predominantly aerobic muscular training, but not by static muscular training. These structural adaptations are confined to those arteries supplying exercising muscle groups, whereas functional adaptations with an improvement of regional compliance are found in all arteries.

This blog is about making athletes think about their training, why do certain things and what happens when we try to adapt training programmes to our physiology instead of following the normal cookie cutter approach of just doing. Understanding what functional and structural changes are helps with this understanding of why we see certain changes through training. There is no official definition and these ideas come from FaCT so I have made my own version of the definition here plus given a few examples so you can get a idea of what functional and structural training is.

Don't confuse the definitions of functional training (or functional strength training) which Wiki writes it as, training the body for activities of daily life, which in short is transferring the strengths from one movement with resistance to a sport or activity.

Functional change definition: This is normally a short term result of training and is where the initial changes in the body is seen. Functional changes are often temporary and is gained and lost quickly.

Structural change definition: This is a long term change in the body that results from starting as a functional change and through months and sometimes years of specific training to develop that specific system may see the development of a structural change which supports the human body.

So when the two definition are combined then functional and structural training implies to the development of the human body through specific training which will normally start with functional change, and through specific stresses and adaptions lead to a structural change which will improve athletic performance. The development of the structure of the body which broadly speaking will include the respiratory system, cardiac system, muscular system, hormones, blood system etc.

Here are some simple examples: A professional cyclist who has been cycling for years, has a higher amount of mitochondria growth and capillarization compared to a amateur. Using the same trained cyclist, his muscles have developed from being a amateur cyclist being functionally good to adjusting the muscle fibres structurally so that they can better perform the required activity.

Athletes thus in general have a higher ability to utilise oxygen and pump a higher volume of blood which is developed through training.

You say so what, this is obvious. Here are some more examples to think through: A novice cross country skier will have problems initially learning to ski and use a huge amount of energy learning to balance, after a few days he has learned to balance and found the needed coordination and he will be skiing faster simply by having made a functional change. Now you did some tests as he started skiing and a few weeks later the skier has shown an improvement and you think, great he is fitter, but most likely due to the improved balance and coordination the skier is able to use more muscle to ski faster, which may show a higher VO2, instead of using muscle to balance. The Skier will initially very quickly develop the utilisation ability through capillarization and mitochondria density and the before mentioned improved balance and co-ordination. This is often the big improvements seen in research studies which last only a few weeks versus trained athletes where changes are small as there is very little room for functional changes. To make structural changes which will strengthen the athletes respiratory system, improve cardiac output and stroke volume may take months or even years.

Another type of example: A athlete goes to altitude or sleeps in a altitude tent and is able to raise his blood values, now he goes back to a lower altitude to compete and if he is a responder to altitude, he/her body is simply utilising the extra oxygen available to the body. To make a real altitude adaption takes many years of IHT and altitude training where the body learns to adapt, and to better utilize and deliver.

Some individuals can improve Stroke Volume (SV) through certain training protocols or even exercise which can be due to a plasma volume increase. This again is a very functional change which is temporary. Repeating this functional training over several weeks, sometimes months should (if the correct stimulus is used with the correct timing to stress the limitation) see a structural change in End Diastolic Volume (EDV) as a change in heart size, thus a higher volume ability to pump blood (stroke volume) and a lower heart rate (CO=SVxHR).

So in any system that you are training you need to think, is it development or just utilisation, i.e. capillarization or capillary utilisation, SV through plasma expansion or SV through EDV improvement, mitochondria density or mitochondria enzyme reaction. Is the sudden improvement weather related, (hot=warmer tarmac=different reactions on bicycle/skate wheels resistance.) or is it true structural adaptation. Another improvement which has not even been mentioned is on the mental side. Once you have done lets say a performance test, you know how it feels, so next time in most cases without any physical improvement you know how to pace it better. Changes in nutrition can make functional changes to blood (e.g. beet root) certain supplements which may buffer H+. Respiratory training with specific devices will initially show great improvements as coordination and general conditioning improves (similar to the idea with the skier) but long term diaphragm strength and transfer of training to sport specific activity may take months.

The key to train structure, you need to find what is the limitation which is creating the weak link in athletic performance.

Thank you Juerg...as you can see beginner can get fairly crazy pretty quickly...after I posted my response of questions I reread what I had written (again) and realized I was asking questions that "sort of" pertained to the analysis but not really...so I wall try to stay on interpreting the information and figuring out the limiter...

Basically, we can perhaps come up with rough zoning ideas with SmO2 only but it isn't until we add the tHb that we can start to sort out the why?

And was the interpretation of the speed check correct? (please give me that one)...

So once we add tHb, we can start to toy around with the idea of figuring out the compensator and limiter...especially with a second or third moxy in place and maybe more info (HR, resp)?

Can you define a couple of terms for me to make sure we are on the same page...at the start of the advanced interpretation, you discuss vasoconstriction...and you state that it can be cause by two things, 1 being mechanical and then you don't mention the other...my questions are in bold trying to piece together what is happening at the start of each new step or at high intensity

A decrease in tHb could be named vasoconstriction or reduction in blood flow. Vasoconstriction can have in simple terms 2 reasons. 1. Mechanical reason . like muscle contraction so we compress the blood vessels and we reduce blood flow so tHb drops ( similar like when we inflate a BP cuff.. So we have first a reduce v blood flow so tHb drops.Is this due to arterial occlusion when muscle first contracts or high contraction force?If we keep pumping upHow because we have a reduction in blood flow? we half suddenly a pressure , which stops outflow venous occlusion or at least reduces outflow, so despite a initial compression we now may see an increase in tHb as blood still moves in but less or nothing moves out..So now in this situation we have an increase in tHb because we have a venous occlusion but not an arterial occlusion? which come first? If we let go the cuff or muscle compression than we see a drop as we have now first a pooling outflow before we are back to " normal " flow. If we even increase more we may reach an in and anyway outflow pressure and now tHb is flat. ( so it looks like normal but when we let go we see first a drop as again an outflow ( some exceptions ).There is one more easy way to see, whether it is a complete occlusion or free flow. Look and think what you may expect SmO2 would do under complete occlusion versus free flow.My guess is that it would drop, no blood moving in or out but O2 being used

Dan. Thanks for insisting. I often miss answers or points so ye s come always back. So let's see where i got lost as usual. a )

And was the interpretation of the speed check correct? (please give me that one)...and the original summary ? Now for vascularization development, I read on the forum or in the pdf's that training at the highest point of SmO2 would be valuable...why not at the highest intensity of the STEI zone?...is it the high O2 content within the muscle that triggers the stimulus for capillarization...then how about mitochondrial density?...why not the highest intensity of STEI zone therefore putting a stress on enzymatic activity, mitochondrial activity?

The answer is often not that clear even when we often get straight forward intensities for this. I believe we have to look at the different situations who ask for limitations and compensations. Vascularisation can perhaps even be called angiogenesis or new build ups of blood vessels. The actual reasons or triggers to this steps is not well know but we have different theories. For mechanical forces over chemical reactions and more. Than there is the big big discussion whether the " recruitment" of blood vessels is really as we all learn or learned. Here the old idea in a picture we often as well show in presentations. Whne I checked d my last presentation I had to ask my self, is this really up to date or is it just a nice way to avoid questions on this topic as it looks so logic. Here what i mean.

This is what I normally used as a part of the physiological reactions. It was simple clear and made some sense and I like all of us had to believe, what the researcher would come up with. I over all this years never got challenged on this one even If I had top Ph. D guys in the courses. I hate that as I am sure we always have to challenge in one or the other way, when there are some open questions. So I was digging around as the idea was just too nice to be completely true. No Problem . I do not have an answer anymore. Here why.

And here the new picture I use together with the old one ?

Than we add functional and structural challenge and reactions and we have even more open questions. So my answer for myself is: I have no clue anymore. So what I do I assess with what I have and if it is one MOXY I use one moxy if I have other additional tools great I can add them as well. Now when the assessment suggest a capillarisation limitation I try different approaches. a) I make a short term plasma volume expansion workout and see, whether I have a different reaction the next day due to the short term functional increase in CO . A capillarsiation limitation can show up as a basic calibration tHb value of let's say 12. than during a workout or assessment when I suddenly stop the load but keep CO up , I can see, whether I easy overshoot today 12 tHb value as a sign of an increase in blood flow in the tested area. A limitation in capillarisation will often show a minimal increase after I get rid of muscle compression as most of the vessels are alread open or circulated. Hope this makes sense.

Next upyou discuss vasoconstriction...and you state that it can be cause by two things, 1 being mechanical and then you don't mention the other.

H aha see that is me start out nicely and forget the end: 1.Mechanical. and here I mean different mechanical or outside pressure. Physiological mechanical is most often the actual muscle contraction compression. It shows up in tHb as a drop in the trace. If after the initial muscle compression like you start running or rowing or any activity the now " balance" muscle activity is slightly lower in strength or motor unit recruitment you than have a decompression to the now actual blood flow.

Above an example who could show that initial drop followed by a decompression reaction in tHb. If . the muscle contraction force is strong or may get even stronger, than you will see an increase in tHb as well after the initial drop, but now it is NOT a decompression but a start or a complete venous occlusion or outflow restriction and tHb goes up. Again if you keep increasing your force you may see a stop in tHB increase as you reach an arterial or complete occlusion. Now you will have a different situation, as you let go and you have an outflow from the pooled blood.. See below a biceps contraction picture. Important. If you read studies on occlusions it is not a physiological occlusion but it is an artificial occlusion over a cuff. If this is done perfect you will have no outflow of tHb but instantly a venous or arterial occlusion

Now other mechanical compression can be from clothing. That's why we do not like bandage or circular options to mount a NIRS. Compression stockings is an other mechanical compression so we do not like to use compression sleeves for NIRS assessment. Another mechanical reason is positioning. Like how a player in an off ice section sits or stands on the bench. Or how a rower in the start situation hold his legs or when you change from an upper handle bar position to an aero position and so on. Even in a bike test 6 or 12 0 clock position of your leg ( try it out. ) Now besides mechanical tHb reactions we have physiological tHb reactions. The most common two are: Vasodilatation due to increase in CO or CO2 and vasoconstriction due to reflex reactions like BP correction. Here an old paper but a very nice one

Okay next section on Dan's part :So now in this situation we have an increase in tHb because we have a venous occlusion but not an arterial occlusion? which come first? Think as in blood pressure you have an upper and lower BP. so when you reach the lower BP resistance you have no outflow anymore and you can feel that in your arm as you reached venous BP , than once you reach arterial pressure ( upper pressure ) you stop inflow as well so you have no flow anymore. So venous before arterial.

2. My guess is that it would drop, no blood moving in or out but O2 being usedThis is Dan's great feedback on what happens in an arterial occlusion with SmO2 to a free flow on SmO2.

Now here a fun home experiment.

The " classical " idea is, that when you do a one or 2 rep muscle activity like lets' say a bicep s curl. That for this one or 2 reps you do not use O2 or in other terms it is completely anaerobic alacticid. Now if that is true we do not need O2 for that ??? So make an occlusion with a band on your upper arm just above biceps and have a MOXY on your biceps or forearm or both. Now simply wait as you have no inflow anymore but your cells or who ever still will use O2. So you will see SmO2 dropping slowly but surely and you do nothing. Now once your each perhaps not even zero but 10 start doing your 1 or 2 rep weight with biceps and tell us on here how you did it , where you able to do it and if you do any other loads can you do it as long it is " anaerobe so up to perhaps 6 loads. .

Remember the discussion o HIT and ts surprisingly good result on O2 usage compared with LSD. Well HIT is highly aerobic and uses per time unit much more O2 than LSD . So it is not what we learned , anaerobic alacticid, but highly aerobic and high lacticid . So no wonder we have a similar functional reaction but even much better than doing an LSD workout. We train functionally a much more e and more intense O2 usage and recovery of CrP where we need O2 as well. SmO2 can be used as a indirect feedback on your CrP recovery. STF fibers have a much faster SmO2 recovery than FTF fibers. We come back later on that one as well. The question: How did we find out the difference in recovery of STF and FTF without using a biopsy .?

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